International medical case reports journal · 2026
Dupilumab for Atopic Dermatitis-Associated Nail Dystrophy: A Case Report.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhao Zexin, Li Hongxia, Luo Deping, Guan Liancheng, Yang Fan
Аннотация
BACKGROUND: Nail dystrophy is a frequently overlooked manifestation of atopic dermatitis (AD). Although studies suggest a pooled prevalence of up to 11%, nail changes-particularly in the absence of active eczema-are often misdiagnosed as onychomycosis, leading to ineffective antifungal therapy. Evidence regarding targeted biologic treatment for this isolated phenotype remains scarce.
CASE PRESENTATION: We report a 57-year-old woman with a 10-year history of AD who developed progressive dystrophy of five fingernails over 2 years. She was repeatedly diagnosed with onychomycosis and treated with several courses of topical naftifine-ketoconazole and systemic itraconazole, without clinical benefit. Physical examination revealed markedly thickened, yellow-brown nail plates with periungual erythema and edema, but no active generalized eczema. Serial direct microscopy and fungal cultures after adequate antifungal washout were consistently negative, while total serum IgE was markedly elevated and a strong family history of atopy was present. After exclusion of other causes of nail dystrophy, a diagnosis of AD-associated nail dystrophy was established. Dupilumab was initiated with a 600 mg loading dose followed by 300 mg subcutaneously every 2 weeks, resulting in gradual improvement, complete resolution of periungual inflammation by week 12, and full nail plate reconstruction by week 28. At the 52-week follow-up, the nail plates remained largely normal with only mild roughness, without recurrence or new adverse events, while maintenance therapy with dupilumab was continued.
CONCLUSION: This case illustrates that AD-related nail dystrophy should be considered in patients with chronic nail changes, negative mycological studies, elevated total serum IgE, and a personal or family history of atopy. Dupilumab achieved complete and durable resolution of nail dystrophy in this patient, supporting IL-4/IL-13 pathway inhibition as a rational therapeutic option for this challenging phenotype of AD.
CASE PRESENTATION: We report a 57-year-old woman with a 10-year history of AD who developed progressive dystrophy of five fingernails over 2 years. She was repeatedly diagnosed with onychomycosis and treated with several courses of topical naftifine-ketoconazole and systemic itraconazole, without clinical benefit. Physical examination revealed markedly thickened, yellow-brown nail plates with periungual erythema and edema, but no active generalized eczema. Serial direct microscopy and fungal cultures after adequate antifungal washout were consistently negative, while total serum IgE was markedly elevated and a strong family history of atopy was present. After exclusion of other causes of nail dystrophy, a diagnosis of AD-associated nail dystrophy was established. Dupilumab was initiated with a 600 mg loading dose followed by 300 mg subcutaneously every 2 weeks, resulting in gradual improvement, complete resolution of periungual inflammation by week 12, and full nail plate reconstruction by week 28. At the 52-week follow-up, the nail plates remained largely normal with only mild roughness, without recurrence or new adverse events, while maintenance therapy with dupilumab was continued.
CONCLUSION: This case illustrates that AD-related nail dystrophy should be considered in patients with chronic nail changes, negative mycological studies, elevated total serum IgE, and a personal or family history of atopy. Dupilumab achieved complete and durable resolution of nail dystrophy in this patient, supporting IL-4/IL-13 pathway inhibition as a rational therapeutic option for this challenging phenotype of AD.